Cell Type–Specific Loss of BDNF Signaling Mimics Optogenetic Control of Cocaine Reward

Author:

Lobo Mary Kay1,Covington Herbert E.1,Chaudhury Dipesh2,Friedman Allyson K.2,Sun HaoSheng1,Damez-Werno Diane1,Dietz David M.1,Zaman Samir1,Koo Ja Wook1,Kennedy Pamela J.1,Mouzon Ezekiell1,Mogri Murtaza3,Neve Rachael L.4,Deisseroth Karl3,Han Ming-Hu12,Nestler Eric J.12

Affiliation:

1. Fishberg Department of Neuroscience, Mount Sinai School of Medicine, New York, NY 10029, USA.

2. Pharmacology and System Therapeutics, Mount Sinai School of Medicine, New York, NY 10029, USA.

3. Department of Bioengineering, Stanford University, Stanford, CA 94305, USA.

4. Department of Brain and Cognitive Sciences, Massachusetts Institute of Technology, Cambridge, MA 02139, USA.

Abstract

BDNF, Dopamine, and Cocaine Reward The nucleus accumbens plays a crucial role in mediating the rewarding effects of drugs of abuse. Different subpopulations of nucleus accumbens projection neurons exhibit balanced but antagonistic influences on their downstream outputs and behaviors. However, their roles in regulating reward behaviors remains unclear. Lobo et al. (p. 385 ) evaluated the roles of the two subtypes of nucleus accumbens projection neurons, those expressing dopamine D1 versus D2 receptors, in cocaine reward. Deleting TrkB, the receptor for brain-derived neurotrophic factor, selectively in each cell type, and selectively controlling the firing of each cell type using optogenetic techniques allowed for confirmation that D1- and D2-containing neurons produced opposite effects on cocaine reward.

Publisher

American Association for the Advancement of Science (AAAS)

Subject

Multidisciplinary

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